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Review
Nature Reviews Immunology 9, 440–447 (1 June 2009) | doi:10.1038/nri2548
A molecular trio in relapse and remission in multiple sclerosis
Abstract
Two thirds of patients with multiple sclerosis have the relapsing-remitting form, which often progresses to more debilitating disease. Striking clinical recovery, termed remission, often follows these periodic neurological defects, termed relapses. Recent work has revealed the role of three key molecules in relapse and remission: α4β1 integrin (also known as VLA4) is an adhesion molecule that mediates T cell migration from the blood into the brain; osteopontin binds to α4β1 integrin, stimulating the production of pro-inflammatory cytokines and inhibiting apoptosis; and αB crystallin inhibits inflammation in the brain. This Review discusses how this molecular trio interacts to initiate relapses (in the case of osteopontin and α4β1 integrin) and then to terminate them as remissions in multiple sclerosis (in the case of αB crystallin).
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